AGC1 and AGC2 export aspartate from mitochondria in exchange for cytosolic glutamate and a proton.
The kinetic properties of AGCs were extensively studied in proteoliposomes.
AGCs participate to cellular REDOX homeostasis and the calcium-mediated control of mitochondrial respiration via the malate-aspartate shuttle.
AGCs gene deficiencies are responsible for rare diseases.
AGC1 is central to neuronal physiology and also plays a role in glutamate-induced excitotoxicity.
AGCs are overexpressed in several types of human tumors.
In silico and in vitro screenings of chemical libraries for identifying new AGC pharmacological modulators are in progress